# Primary National Ambient Air Quality Standard for Sulfur Dioxide > Briefs, arguments, decisions, and more. URL: https://www.frixlaw.com/law-library/documents/fr%3AE9-28058 ## Record - **Collection:** Federal Register - **Document type:** Proposed Rule - **Published:** December 8, 2009 - **Citation:** 74 FR 64810 ## Text ENVIRONMENTAL PROTECTION AGENCY 40 CFR Parts 50, 53, and 58 [EPA-HQ-OAR-2007-0352; FRL-8984-3] RIN 2060-A048 Primary National Ambient Air Quality Standard for Sulfur Dioxide AGENCY: Environmental Protection Agency (EPA). ACTION: Proposed rule. SUMMARY: Based on its review of the air quality criteria for oxides of sulfur and the primary national ambient air quality standard (NAAQS) for oxides of sulfur as measured by sulfur dioxide (SO 2 ), EPA is proposing to revise the primary SO 2 NAAQS to provide requisite protection of public health with an adequate margin of safety. Specifically, EPA proposes to establish a new 1-hour SO 2 standard within the range of 50-100 parts per billion (ppb), based on the 3-year average of the annual 99th percentile (or 4th highest) of 1-hour daily maximum concentrations. The EPA also proposes to revoke both the existing 24-hour and annual primary SO 2 standards. DATES: Comments must be received on or before February 8, 2010. Under the Paperwork Reduction Act, comments on the information collection provisions must be received by OMB on or before January 7, 2010. Public Hearings: A public hearing is scheduled for this proposed rule. The public hearing will be held on January 5, 2010 in Atlanta, Georgia. ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-OAR-2007-0352 by one of the following methods: • http://www.regulations.gov: Follow the on-line instructions for submitting comments. • E-mail: a-and-r-Docket@epa.gov. • Fax: 202-566-9744. • Mail: Docket No. EPA-HQ-OAR-2007-0352, Environmental Protection Agency, Mail Code 6102T, 1200 Pennsylvania Ave., NW., Washington, DC 20460. Please include a total of two copies. • Hand Delivery: Docket No. EPA-HQ-OAR-2007-0352, Environmental Protection Agency, EPA West, Room 3334, 1301 Constitution Ave., NW, Washington, DC. Such deliveries are only accepted during the Docket's normal hours of operation, and special arrangements should be made for deliveries of boxed information. Public Hearings: A public hearing is scheduled for this proposed rule. The public hearing will be held on January 5, 2010 in Atlanta, Georgia. The hearing will be held at the following location: Sam Nunn Atlanta Federal Center, Conference Rooms B and C, 61 Forsyth Street, SW., Atlanta, GA 30303, Telephone: (404) 562-9077. Note: All persons entering the Atlanta Federal Center must have a valid picture ID such as a Driver's License and go through Federal security procedures. All persons must go through a magnetometer and all personal items must go through x-ray equipment, similar to airport security procedures. After passing through the equipment, all persons must sign in at the guard station and show their picture ID. See the SUPPLEMENTARY INFORMATION under “Public Hearing” for further information. Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-2007-0352. EPA's policy is that all comments received will be included in the public docket without change and may be made available online at www.regulations.gov, including any personal information provided, unless the comment includes information claimed to be Confidential Business Information (CBI) or other information whose disclosure is restricted by statute. Do not submit information that you consider to be CBI or otherwise protected through www.regulations.gov or e-mail. The www.regulations.gov Web site is an “anonymous access” system, which means EPA will not know your identity or contact information unless you provide it in the body of your comment. If you send an e-mail comment directly to EPA without going through www.regulations.gov your e-mail address will be automatically captured and included as part of the comment that is placed in the public docket and made available on the Internet. If you submit an electronic comment, EPA recommends that you include your name and other contact information in the body of your comment and with any disk or CD-ROM you submit. If EPA cannot read your comment due to technical difficulties and cannot contact you for clarification, EPA may not be able to consider your comment. Electronic files should avoid the use of special characters, any form of encryption, and be free of any defects or viruses. For additional information about EPA's public docket visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm. Docket: All documents in the docket are listed in the www.regulations.gov index. Although listed in the index, some information is not publicly available, e.g., CBI or other information whose disclosure is restricted by statute. Certain other material, such as copyrighted material, will be publicly available only in hard copy. Publicly available docket materials are available either electronically in www.regulations.gov or in hard copy at the Air and Radiation Docket and Information Center, EPA/DC, EPA West, Room 3334, 1301 Constitution Ave., NW., Washington, DC. The Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The telephone number for the Public Reading Room is (202) 566-1744 and the telephone number for the Air and Radiation Docket and Information Center is (202) 566-1742. FOR FURTHER INFORMATION CONTACT: Dr. Michael J. Stewart, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail Code C504-06, Research Triangle Park, NC 27711; telephone: 919-541-7524; fax: 919-541-0237; e-mail: stewart.michael@epa.gov. SUPPLEMENTARY INFORMATION: General Information What Should I Consider as I Prepare My Comments for EPA? 1. Submitting CBI. Do not submit this information to EPA through www.regulations.gov or e-mail. Clearly mark the part or all of the information that you claim to be CBI. For CBI information in a disk or CD-ROM that you mail to EPA, mark the outside of the disk or CD-ROM as CBI and then identify electronically within the disk or CD-ROM the specific information that is claimed as CBI. In addition to one complete version of the comment that includes information claimed as CBI, a copy of the comment that does not contain the information claimed as CBI must be submitted for inclusion in the public docket. Information so marked will not be disclosed except in accordance with procedures set forth in 40 CFR part 2. 2. Tips for Preparing Your Comments. When submitting comments, remember to: • Identify the rulemaking by docket number and other identifying information (subject heading, Federal Register date and page number). • Follow directions—the agency may ask you to respond to specific questions or organize comments by referencing a Code of Federal Regulations (CFR) part or section number. • Explain why you agree or disagree, suggest alternatives, and substitute language for your requested changes. • Describe any assumptions and provide any technical information and/or data that you used. • Provide specific examples to illustrate your concerns, and suggest alternatives. • Explain your views as clearly as possible, avoiding the use of profanity or personal threats. • Make sure to submit your comments by the comment period deadline identified. Availability of Related Information A number of the documents that are relevant to this rulemaking are available through EPA's Office of Air Quality Planning and Standards (OAQPS) Technology Transfer Network (TTN) Web site at http://www.epa.gov/ttn/naaqs/standards/so2/s_so2_index.html. These documents include the Integrated Review Plan and the Health Assessment Plan, available at, the Integrated Science Assessment (ISA), available at http://www.epa.gov/ttn/naaqs/standards/so2/s_so2_cr_isa.html, and the Risk and Exposure Assessment (REA), available at http://www.epa.gov/ttn/naaqs/standards/so2/s_so2_cr_rea.html. These and other related documents are also available for inspection and copying in the EPA docket identified above. Public Hearing The public hearing on January 5, 2010 will provide interested parties the opportunity to present data, views, or arguments concerning the proposed rule. The EPA may ask clarifying questions during the oral presentations, but will not respond to the presentations at that time. Written statements and supporting information submitted during the comment period will be considered with the same weight as any oral comments and supporting information presented at the public hearing. Written comments must be received by the last day of the comment period, as specified in this proposed rulemaking. The public hearing will begin at 10 a.m. and continue until 7 p.m. (local time) or later, if necessary, depending on the number of speakers wishing to participate. The EPA will make every effort to accommodate all speakers that arrive and register before 7 p.m. A lunch break is scheduled from 12:30 p.m. until 2 p.m. If you would like to present oral testimony at the hearing, please notify Ms. Tricia Crabtree (C504-02), U.S. EPA, Research Triangle Park, NC 27711. The preferred method for registering is by e-mail ( crabtree.tricia@epa.gov ). Ms. Crabtree may be reached by telephone at (919) 541-5688. She will arrange a general time slot for you to speak. The EPA will make every effort to follow the schedule as closely as possible on the day of the hearing. Oral testimony will be limited to five (5) minutes for each commenter to address the proposal. We will not be providing equipment for commenters to show overhead slides or make computerized slide presentations unless we receive special requests in advance. Commenters should notify Ms. Crabtree if they will need specific audiovisual (AV) equipment. Commenters should also notify Ms. Crabtree if they need specific translation services for non-English speaking commenters. The EPA encourages commenters to provide written versions of their oral testimonies either electronically on computer disk, CD-ROM, or in paper copy. The hearing schedule, including lists of speakers, will be posted on EPA's Web site for the proposal at http://www.epa.gov/ttn/naaqs/standards/so2/s_so2_index.html prior to the hearing. Verbatim transcripts of the hearing and written statements will be included in the rulemaking docket. Table of Contents The following topics are discussed in this preamble: I. Background A. Legislative requirements B. Related SO 2 control programs C. History of reviews of the primary NAAQS for sulfur oxides II. Rationale for proposed decisions on the primary standards A. Characterization of SO 2 air quality 1. Anthropogenic sources and current patterns of SO 2 air quality 2. SO 2 monitoring B. Health effects information 1. Respiratory effects and 5-10 minute exposure to SO 2 a. Respiratory symptoms b. Lung function decrements c. Adversity of 5-10 minute respiratory effects 2. Respiratory effects and 1 to 24-hour exposures to SO 2 a. Respiratory symptoms b. Emergency department visits and hospitalizations 3. ISA conclusions regarding short-term (5-minutes to 24-hour) SO 2 exposures 4. Health effects and long-term exposures to SO 2 5. SO 2 -related impacts on public health a. Pre-existing respiratory disease b. Genetics c. Age d. Time spent outdoors e. Ventilation rate f. Socioeconomic status g. Size of at-risk population C. Human exposure and health risk characterization 1. Evidence base for the risk characterization 2. Overview of approaches 3. Key limitations and uncertainties D. Considerations in review of the standards 1. Background on the current standards 2. Approach for reviewing the need to retain or revise the current standards E. Adequacy of the current standards 1. Adequacy of the current 24-hour standard a. Evidence-based considerations b. Air quality, exposure, and risk-based considerations c. Summary of considerations from the REA regarding the 24-hour standard 2. Adequacy of the current annual standard a. Evidence-based considerations b. Air quality, exposure, and risk-based considerations c. Summary of considerations from the REA regarding the annual standard 3. CASAC views regarding adequacy of the current 24-hour and annual standards 4. Administrator's conclusions regarding adequacy of the current 24-hour and annual standards F. Conclusions on the elements of a proposed new short-term standard 1. Indicator 2. Averaging time a. Evidence and air quality, exposure, and risk-based considerations b. CASAC views c. Administrator's conclusions on averaging time 3. Form a. Evidence, air quality, and risk-based considerations b. CASAC views c. Administrator's conclusions on form 4. Level a. Evidence-based considerations b. Air quality, exposure and risk-based considerations c. Observations based on evidence and risk-based considerations d. CASAC views e. Administrator's conclusions on level for a 1-hour standard 5. Implications for retaining or revoking current standards G. Summary of proposed decisions on primary standards III. Proposed Amendments to Ambient Monitoring and Reporting Requirements A. Monitoring methods 1. Background 2. Proposed new FRM measurement technique 3. Technical description of the proposed UVF FRM 4. Implications to air monitoring networks 5. Proposed revisions to 40 CFR Part 53 B. Network design 1. Background 2. Proposed changes a. Population Weighted Emissions Index (PWEI) Triggered Monitoring b. State-level emissions triggered monitoring c. Monitor placement and siting d. Monitoring required by the Regional Administrator e. Alternative Network Design C. Data Reporting IV. Proposed Appendix T—Interpretation of the Primary NAAQS for Oxides of Sulfur and Proposed Revisions to the Exceptional Events Rule A. Background B. Interpretation of the NAAQS for Oxides of Sulfur 1. 1-hour standard based on the annual 4th highest daily value form 2. 1-hour primary standard based on the 99th percentile value form C. Exceptional events information submission schedule V. Designations for the SO 2 NAAQS VI. Clean Air Act Implementation Requirements A. How this rule applies to tribes B. Attainment dates 1. Attaining the NAAQS 2. Consequences of failing to attain by the Statutory Attainment Date C. Section 110(a)(2) NAAQS Infrastructure Requirements D. Attainment planning requirements 1. SO 2 Nonattainment area SIP requirements 2. New source review and prevention of significant deterioration requirements 3. General conformity E. Transition from the existing SO 2 NAAQS to a revised SO 2 NAAQS VII. Communication of public health information VIII. Statutory and executive order reviews A. Executive Order 12866: Regulatory Planning and Review B. Paperwork Reduction Act C. Regulatory Flexibility Act D. Unfunded Mandates Reform Act E. Executive Order 13132: Federalism F. Executive Order 13175: Consultation and Coordination with Indian Tribal Governments G. Executive Order 13045: Protection of Children from Environmental Health & Safety Risks H. Executive Order 13211: Actions that Significantly Affect Energy Supply, Distribution or Use I. National Technology Transfer and Advancement Act J. Executive Order 12898: Federal Actions to Address Environmental Justice in Minority Populations and Low-Income Populations References I. Background A. Legislative requirements Two sections of the Clean Air Act (Act or CAA) govern the establishment and revision of National Ambient Air Quality Standards NAAQS. Section 108 of the Act directs the Administrator to identify and list air pollutants that meet certain criteria, including that the air pollutant “in his judgment, cause[s] or contribute[s] to air pollution which may reasonably be anticipated to endanger public health and welfare” and “the presence of which in the ambient air results from numerous or diverse mobile or stationary sources.” CAA section 108 (a)(1)(A) & (B). For those air pollutants listed, section 108 requires the Administrator to issue air quality criteria that “accurately reflect the latest scientific knowledge useful in indicating the kind and extent of all identifiable effects on public health or welfare which may be expected from the presence of [a] pollutant in ambient air * * *” Section 108 (a) (2). Section 109(a) of the Act directs the Administrator to promulgate “primary” and “secondary” NAAQS for pollutants for which air quality criteria have been issued. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on [the air quality] criteria and allowing an adequate margin of safety, are requisite to protect the public health.” 1 Section 109(b)(1). A secondary standard, in turn, must “specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on [the air quality] criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of such pollutant in the ambient air.” 2 Section 109(b)(2) This proposal concerns exclusively the primary NAAQS for oxides of sulfur. 1 The legislative history of section 109 indicates that a primary standard is to be set at “the maximum permissible ambient air level * * * which will protect the health of any [sensitive] group of the population,” and that for this purpose “reference should be made to a representative sample of persons comprising the sensitive group rather than to a single person in such a group.” S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970). 2 EPA is currently conducting a separate review of the secondary SO 2 NAAQS jointly with a review of the secondary NO 2 NAAQS (see http://www.epa.gov/ttn/naaqs/standards/no2so2sec/index.html for more information). The requirement that primary standards include an adequate margin of safety is intended to address uncertainties associated with inconclusive scientific and technical information available at the time of standard setting. It is also intended to provide a reasonable degree of protection against hazards that research has not yet identified. Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (DC Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (DC Cir. 1981), cert. denied, 455 U.S. 1034 (1982). Both kinds of uncertainties are components of the risk associated with pollution at levels below those at which human health effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary standards that include an adequate margin of safety, the Administrator is seeking not only to prevent pollution levels that have been demonstrated to be harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. In addressing the requirement for a margin of safety, EPA considers such factors as the nature and severity of the health effects involved, the size of the at-risk population(s), and the kind and degree of the uncertainties that must be addressed. The selection of any particular approach to providing an adequate margin of safety is a policy choice left specifically to the Administrator's judgment. Lead Industries Association v. EPA, 647 F.2d at 1161-62. In setting standards that are “requisite” to protect public health and welfare, as provided in section 109(b), EPA's task is to establish standards that are neither more nor less stringent than necessary for these purposes. In so doing, EPA may not consider the costs of implementing the standards. Whitman v. American Trucking Associations, 531 U.S. 457, 471, 475-76 (2001). Section 109(d)(1) of the Act requires the Administrator to periodically undertake a thorough review of the air quality criteria published under section 108 and the NAAQS and to revise the criteria and standards as may be appropriate. The Act also requires the Administrator to appoint an independent scientific review committee composed of seven members, including at least one member of the National Academy of Sciences, one physician, and one person representing State air pollution control agencies, to review the air quality criteria and NAAQS and to “recommend to the Administrator any new * * * standards and revisions of existing criteria and standards as may be appropriate under section 108 and subsection (b) of this section.” CAA section 109 (d)(2). This independent review function is performed by the Clean Air Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board. B. Related SO 2 control programs States are primarily responsible for ensuring attainment and maintenance of ambient air quality standards once EPA has established them. Under section 110 of the Act, and related provisions, States are to submit, for EPA approval, State implementation plans (SIPs) that provide for the attainment and maintenance of such standards through control programs directed to sources of the pollutants involved. The States, in conjunction with EPA, also administer the prevention of significant deterioration program that covers these pollutants. See CAA sections 160-169. In addition, Federal programs provide for nationwide reductions in emissions of these and other air pollutants through the Federal motor vehicle and motor vehicle fuel control program under title II of the Act, (CAA sections 202-250) which involves controls for emissions from all moving sources and controls for the fuels used by these sources; new source performance standards under section 111; and title IV of the Act (CAA sections 402-416), which specifically provides for major reductions in SO 2 emissions. EPA has also promulgated the Clean Air Interstate Rule (CAIR) to define additional SO 2 emission reductions needed in the Eastern United States to address the interstate impact provisions of CAA section 110(a)(2)(D), a rule which EPA is reevaluating pursuant to court remand. Currently, there are several areas designated as being in nonattainment of the primary SO 2 NAAQS (see section VI). If the SO 2 NAAQS is revised as a result of this review; however, some additional areas could be classified as non-attainment. Certain States would then be required to develop SIPs that identify and implement specific air pollution control measures to reduce ambient SO 2 concentrations to attain and maintain the revised SO 2 NAAQS, most likely by requiring air pollution controls on sources that emit oxides of sulfur (SO X ). C. History of reviews of the primary NAAQS for sulfur oxides On April 30, 1971, the EPA promulgated primary SO 2 NAAQS (36 FR 8187). These primary standards, which were based on the findings outlined in the original 1969 Air Quality Criteria for Sulfur Oxides, were set at 0.14 parts per million averaged over a 24-hour period, not to be exceeded more than once per year, and 0.030 ppm annual arithmetic mean. In 1982, EPA published the Air Quality Criteria for Particulate Matter and Sulfur Oxides (EPA, 1982) along with an addendum of newly published controlled human exposure studies, which updated the scientific criteria upon which the initial standards were based (EPA, 1982). In 1986, EPA published a second addendum presenting newly available evidence from epidemiologic and controlled human exposure studies (EPA, 1986). In 1988, EPA published a proposed decision not to revise the existing standards (53 FR 14926) (April 26, 1988). However, EPA specifically requested public comment on the alternative of revising the current standards and adding a new 1-hour primary standard of 0.4 ppm (400 ppb) to protect against 5-10 minute peak SO 2 concentrations. As a result of public comments on the 1988 proposal and other post-proposal developments, EPA published a second proposal on November 15, 1994 (59 FR 58958). The 1994 re-proposal was based in part on a supplement to the second addendum of the criteria document, which evaluated new findings on 5-10 minute SO 2 exposures in asthmatics (EPA, 1994a). As in the 1988 proposal, EPA proposed to retain the existing 24-hour and annual standards. EPA also solicited comment on three regulatory alternatives to further reduce the health risk posed by exposure to high 5-minute peaks of SO 2 if additional protection were judged to be necessary. The three alternatives were: (1) Revising the existing primary SO 2 NAAQS by adding a new 5-minute standard of 0.6 ppm (600 ppb) SO 2 ; (2) establishing a new regulatory program under section 303 of the Act to supplement protection provided by the existing NAAQS, with a trigger level of 0.6 ppm (600 ppb) SO 2 , one expected exceedance; and (3) augmenting implementation of existing standards by focusing on those sources or source types likely to produce high 5-minute peak concentrations of SO 2 . On May 22, 1996, EPA announced its final decision not to revise the NAAQS for SO X (61 FR 25566). EPA found that asthmatics (a susceptible population group) could be exposed to such short-term SO 2 bursts resulting in repeated ‘exposure events’ such that tens or hundreds of thousands of asthmatics could be exposed annually to lung function effects “distinctly exceeding * * * [the] typical daily variation in lung function” that asthmatics routinely experience, and found further that repeated occurrences should be regarded as significant from a public health standpoint. 61 FR at 25572, 25573. Nonetheless, the agency concluded that “the likelihood that asthmatic individuals will be exposed * * * is very low when viewed from a national perspective”, that “5-minute peak SO[ 2 ] levels do not pose a broad public health problem when viewed from a national perspective”, and that “short-term peak concentrations of SO[ 2 ] do not constitute the type of ubiquitous public health problem for which establishing a NAAQS would be appropriate.” Id. at 25575. EPA concluded, therefore, that it would not revise the existing standards or add a standard to specifically address 5-minute exposures. EPA also announced an intention to propose guidance, under section 303 of the Act, to assist states in responding to short-term peak of SO 2 and later initiated a rulemaking to do so (62 FR 210 (Jan. 2, 1997). The American Lung Association and the Environmental Defense Fund challenged EPA's decision not to establish a 5-minute standard. On January 30, 1998, the Court of Appeals for the District of Columbia found that EPA had failed to adequately explain its determination that no revision to the SO 2 NAAQS was appropriate and remanded the determination back to EPA for further explanation. American Lung Ass'n v. EPA, 134 F. 3d 388 (DC Cir. 1998). Specifically, the court held that EPA had failed to adequately explain the basis for its conclusion that short-term SO 2 exposures to asthmatics do not constitute a public health problem, noting that the agency had failed to explain the link between its finding that repeated short-term exposures were significant, and that there would be tens to hundreds of thousands of such exposures annually to a susceptible subpopulation, but that a NAAQS was found not be appropriate. 134 F. 3d at 392. The court also rejected the explanation that short-term SO 2 bursts were “localized, infrequent, and site-specific” as a rational basis for the conclusion that no public health problem existed: “[N]othing in the Final Decision explains why ‘localized’, ‘site-specific’, or even ‘infrequent’ events might nevertheless create a public health problem, particularly since, in some sense, all pollution is local and site-specific * * *”. Id. The court accordingly remanded the case to EPA to adequately explain its determination or otherwise take action in accordance with the opinion. In response, EPA has collected and analyzed additional air quality data focused on 5-minute concentrations of SO 2 . These air quality analyses conducted since the last review will help inform the current review, which will address the issues raised in the court's remand of the Agency's last decision. EPA formally initiated the current review of the air quality criteria for oxides of sulfur and the SO 2 primary NAAQS on May 15, 2006 (71 FR 28023) with a general call for information. EPA's draft Integrated Review Plan for the Primary National Ambient Air Quality Standards for Sulfur Dioxide (EPA, 2007a) was made available in April 2007 for public comment and was discussed by the CASAC via a publicly accessible teleconference on May 11, 2007. As noted in that plan, SO X includes multiple gaseous ( e.g., SO 3 ) and particulate ( e.g., sulfate) species. Because the health effects associated with particulate species of SO x have been considered within the context of the health effects of ambient particles in the Agency's review of the NAAQS for particulate matter (PM), the current review of the primary SO 2 NAAQS is focused on the gaseous species of SO x and does not consider health effects directly associated with particulate species. The first draft of the Integrated Science Assessment for Oxides of Sulfur-Health Criteria (ISA) and the Sulfur Dioxide Health Assessment Plan: Scope and Methods for Exposure and Risk Assessment (EPA, 2007b) were reviewed by CASAC at a public meeting held on December 5-6, 2007. Based on comments received from CASAC and the public, EPA developed the second draft of the ISA and the first draft of the Risk and Exposure Assessment to Support the Review of the SO 2 Primary National Ambient Air Quality Standard (Risk and Exposure Assessment (REA)). These documents were reviewed by CASAC at a public meeting held on July 30-31, 2008. Based on comments received from CASAC and the public at this meeting, EPA released the final ISA in September of 2008 (EPA, 2008a; henceforth referred to as ISA). In addition, comments received were considered in developing the second draft of the REA. Importantly, the second draft of the REA contained a draft staff policy assessment that considered the evidence presented in the final ISA and the air quality, exposure, and risk characterization results presented in the second draft REA, as they related to the adequacy of the current SO 2 NAAQS and potential alternative primary SO 2 standards. This document was reviewed by CASAC at a public meeting held on April 16-17, 2009. In preparing the final REA report, which included the final staff policy assessment, EPA considered comments received from CASAC and the public at and subsequent to that meeting. The final REA containing the final staff policy assessment was completed in August 2009 (EPA 2009a; henceforth referred to as REA). The schedule for completion of this review is governed by a judicial order resolving a lawsuit filed in September 2005, concerning the timing of the current review. Center for Biologic Diversity v. Johnson (Civ. No. 05-1814) (D.D.C. 2007). The order that now governs this review, entered by the court in August 2007 and amended in December 2008, provides that the Administrator will sign, for publication, notices of proposed and final rulemaking concerning the review of the primary SO 2 NAAQS no later than November 16, 2009 and June 2, 2010, respectively. This action presents the Administrator's proposed decisions on the current primary SO 2 standards. Throughout this preamble a number of conclusions, findings, and determinations proposed by the Administrator are noted. Although they identify the reasoning that supports this proposal, they are not intended to be final or conclusive. EPA invites general, specific, and/or technical comments on all issues involved with this proposal, including all such proposed judgments, conclusions, findings, and determinations. In addition to requesting comment on the overall approach, EPA invites specific comment on the level, or range of levels, appropriate for such a standard, as well as on the rationale that would support that level or range of levels. II. Rationale for proposed decisions on the primary standards This section presents the rationale for the Administrator's proposed decision to revise the existing SO 2 primary standards by replacing the current 24-hour and annual standards with a 1-hour standard and to specify this 1-hour standard to the nearest parts per billion (ppb). As discussed more fully below, this rationale takes into account: (1) Judgments and conclusions presented in the ISA and the REA; (2) CASAC advice and recommendations, as reflected in the CASAC panel's discussions of drafts of the ISA and REA at public meetings, in separate written comments, and in CASAC letters to the Administrator (Henderson 2008; Samet, 2009); and (3) public comments received at CASAC meetings during the development of the ISA and the REA. In developing this rationale, EPA has drawn upon an integrative synthesis of the entire body of evidence on human health effects associated with the presence of SO 2 in the ambient air, and upon the results of quantitative exposure and risk assessments reflecting this evidence. As discussed below, this body of evidence addresses a broad range of health endpoints associated with exposure to SO 2 in the ambient air. In considering this entire body of evidence, EPA chose to focus in particular on those health endpoints for which the ISA finds associations with SO 2 to be causal or likely causal (see section II.B below). Thus, the focus of this proposal will be on respiratory morbidity following short-term (5 minutes to 24 hours) exposure to SO 2 , for which the ISA found a causal relationship. As discussed below, a substantial amount of new research has been conducted since EPA's last review of the SO 2 NAAQS, with important new information coming from epidemiologic studies in particular. The newly available research studies evaluated in the ISA have undergone intensive scrutiny through multiple layers of peer review and opportunities for public review and comment. Although important uncertainties remain in the qualitative and quantitative characterizations of health effects attributable to exposure to ambient SO 2 , the review of this information has been extensive and deliberate. The remainder of this section discusses the Administrator's rationale for the proposed decisions on the primary standard. Section II.A presents a discussion of the principal emitting sources and current patterns of SO 2 air quality, as well as the current SO 2 monitoring network from which those air quality patterns are obtained. Section II.B includes an overview of the scientific evidence related to the respiratory effects associated with ambient SO 2 exposure. This overview includes a discussion of the at-risk populations considered in the ISA. Section II.C discusses the approaches taken by EPA to assess exposures and health risks associated with exposure to ambient SO 2 , including a discussion of key uncertainties associated with the analyses. Section II.D presents the approach that is being used in the current review of the SO 2 NAAQS with regard to consideration of the scientific evidence and the air quality, exposure, and risk-based results related to the adequacy of the current standards and potential alternative standards. Sections II.E and II.F discuss the scientific evidence and the air quality, exposure, and risk-based results specifically as they relate to the current and potential alternative standards, including discussion of the Administrator's proposed decisions on the standards. Section II.G summarizes the Administrator's proposed decisions with regard to the SO 2 primary NAAQS. A. Characterization of SO 2 air quality 1. Anthropogenic sources and current patterns of SO 2 Air Quality Anthropogenic SO 2 emissions originate chiefly from point sources, with fossil fuel combustion at electric utilities (~66%) and other industrial facilities (~29%) accounting for the majority of total emissions (ISA, section 2.1). Other anthropogenic sources of SO 2 include both the extraction of metal from ore as well as the burning of high sulfur-containing fuels by locomotives, large ships, and equipment utilizing diesel engines. SO 2 emissions and ambient concentrations follow a strong east to west gradient due to the large numbers of coal-fired electric generating units in the Ohio River Valley and upper Southeast regions. In the 12 Consolidated Metropolitan Statistical Areas (CMSAs) that had at least four SO 2 regulatory monitors from 2003-2005, 24-hour average concentrations in the continental U.S. ranged from a reported low of ~1 ppb in Riverside, CA and San Francisco, CA to a high of ~12 ppb in Pittsburgh, PA and Steubenville, OH (ISA, section 2.5.1). In addition, outside or inside all CMSAs from 2003-2005, the annual average SO 2 concentration was 4 ppb (ISA, Table 2-8). However, spikes in hourly concentrations occurred; the mean 1-hour maximum concentration outside or inside CMSAs was 13 ppb, with a maximum value of greater than 600 ppb outside CMSAs and greater than 700 ppb inside CMSAs (ISA, Table 2-8). Temporal and spatial patterns of 5-minute peaks of SO 2 are also important given that human clinical studies have demonstrated that exposure to these peaks can result in adverse respiratory effects in exercising asthmatics (see section II.B). For those monitors which voluntarily reported 5-minute block average data, 3 when maximum 5-minute concentrations were reported, the absolute highest concentration over the ten-year period exceeded 4000 ppb, but for all individual monitors, the 99th percentile was below 200 ppb (ISA, section 2.5.2 Table 2-10). Median concentrations from these monitors reporting 5-minute data ranged from 1 ppb to 8 ppb, and the average for each maximum 5-minute level ranged from 3 ppb to 17 ppb. Delaware, Pennsylvania, Louisiana, and West Virginia had mean values for maximum 5-minute data exceeding 10 ppb. Among aggregated within-state data for the 16 monitors from which all 5-minute average intervals were reported, the median values ranged from 1 ppb to 5 ppb, and the means ranged from 3 ppb to 11 ppb (ISA, section 2.5.2). The highest reported concentration was 921 ppb, but the 99th percentile values for aggregated within-state data were all below 90 ppb (ISA, section 2.5.2). 3 A small number of sites, 98 total from 1997 to 2007 of the approximately 500 SO 2 monitors, and not the same sites in all years, voluntarily reported 5-minute block average data to AQS (ISA, section 2.5.2). Of these, 16 reported all twelve 5-minute averages in each hour for at least part of the time between 1997 and 2007. The remainder reported only the maximum 5-minute average in each hour. 2. SO 2 monitoring Although the SO 2 standard was established in 1971, uniform minimum monitoring requirements for SO 2 monitoring did not appear until May 1979. From the time of the implementation of the 1979 monitoring rule through 2008, the SO 2 network has steadily decreased in size from approximately 1496 sites in 1980 to the approximately 488 sites operating in 2008. At present, except for SO 2 monitoring required at National Core Monitoring Stations (NCore stations), there are no minimum monitoring requirements for SO 2 in 40 CFR part 58 Appendix D, other than a requirement for EPA Regional Administrator approval before removing any existing monitors and that any ongoing SO 2 monitoring must have at least one monitor sited to measure the maximum concentration of SO 2 in that area. EPA removed the specific minimum monitoring requirements for SO 2 in the 2006 monitoring rule revisions, based on the fact that there were no SO 2 nonattainment areas at that time, coupled with trends evidence showing an increasing gap between national average SO 2 concentrations and the current 24-hour and annual standards. Additionally, the minimum requirements were removed to provide State, local, and tribal air monitoring agencies flexibility in meeting higher priority monitoring needs for pollutants such as ozone and PM 2.5 , or implementing the new multi-pollutant sites (NCore network) required by the 2006 rule revisions, by allowing them to discontinue lower priority monitoring. More information on SO 2 monitoring can be found in section III. B. Health effects information During the last review, EPA retained the current 24-hour and annual averaging times for the primary SO 2 NAAQS. The 24-hour NAAQS was largely based on epidemiologic studies that observed associations between 24-hour average SO 2 levels and adverse respiratory effects and daily mortality (EPA 1982, 1994a, 1994b). The annual standard was supported by a few epidemiologic studies that found an association between adverse respiratory effects and annual average SO 2 concentrations (EPA 1982, 1994a, 1994b). However, it was noted that in the locations where these epidemiologic studies were conducted, high SO 2 levels were usually accompanied by high levels of PM, thus making it difficult to disentangle the individual contribution each pollutant had on these health outcomes. Moreover, EPA noted that rather than 24-hour or annual average SO 2 levels, the health effects observed in these studies may have been related, at least in part, to the occurrence of shorter-term peaks of SO 2 within a 24-hour period (53 FR 14930; April 26, 1988). In the current review, the ISA along with its associated annexes, provided a comprehensive review and assessment of the scientific evidence related to the health effects associated with SO 2 exposures. For these health effects, the ISA characterized judgments about causality with a hierarchy that contains five levels (ISA, section 1-3): sufficient to infer a causal relationship, sufficient to infer a likely causal relationship ( i.e., more likely than not), suggestive but not sufficient to infer a causal relationship, inadequate to infer the presence or absence of a causal relationship, and suggestive of no causal relationship. Judgments about causality were informed by a series of aspects that are based on those set forth by Sir Austin Bradford Hill in 1965 (ISA, Table 1-1). These aspects include strength of the observed association, availability of experimental evidence, consistency of the observed association, biological plausibility, coherence of the evidence, temporal relationship of the observed association, and the presence of an exposure-response relationship. Judgments made in the ISA about the extent to which relationships between various health endpoints and exposure to SO 2 are likely causal have been informed by several factors. As discussed in the ISA in section 1.3, these factors include the nature of the evidence ( i.e., controlled human exposure, epidemiologic, and/or toxicological studies) and the weight of evidence. The weight of evidence takes into account such considerations as biological plausibility, coherence of the evidence, strength of associations, and consistency of the evidence. Controlled human exposure studies provide directly applicable information for determining causality because these studies are not limited by differences in dosimetry and species sensitivity, which would need to be addressed in extrapolating animal toxicology data to human health effects, and because they provide data relating health effects specifically to SO 2 exposures, in the absence of the co-occurring pollutants present in ambient air. Epidemiologic studies provide evidence of associations between SO 2 concentrations and more serious health endpoints ( e.g., hospital admissions and emergency department visits) that cannot be assessed in controlled human exposure studies. For these studies the degree of uncertainty introduced by confounding variables ( e.g., other pollutants) affects the level of confidence that the health effects being investigated are attributable to SO 2 exposures alone and/or in combination with co-occurring pollutants. In using a weight of evidence approach to inform judgments about the degree of confidence that various health effects are likely to be caused by exposure to SO 2 , confidence increases with the number of studies consistently reporting a particular health endpoint, with increasing support for the biological plausibility of the health effects, and with the strength and coherence of the evidence. Conclusions regarding biological plausibility, consistency, and coherence of evidence of SO 2 -related health effects are drawn from the integration of epidemiologic studies with controlled human exposure studies and with mechanistic information from animal toxicological studies. As discussed below, the weight of evidence is strongest for respiratory morbidity endpoints ( e.g., lung function decrements, respiratory symptoms, hospital admissions, and emergency department visits) associated with short-term (5-minutes to 24-hours) exposure to ambient SO 2 . For epidemiologic studies, strength of association refers to the magnitude of the association and its statistical strength, which includes assessment of both effect estimate size and precision. In general, when associations yield large relative risk estimates, it is less likely that the association could be completely accounted for by a potential confounder or some other bias. Consistency refers to the persistent finding of an association between exposure and outcome in multiple studies of adequate power in different persons, places, circumstances and times. Being mindful of the considerations discussed above, the ISA concluded that there was sufficient evidence to infer a causal relationship between respiratory morbidity and short-term (5-minutes to 24-hours) exposure to SO 2 (ISA, section 5.2). The ISA based this conclusion on the consistency, coherence, and plausibility of findings observed in controlled human exposure studies of 5-10 minutes, epidemiologic studies mostly using 1-hour daily maximum and 24-hour average SO 2 concentrations, and animal toxicological studies using exposures of minutes to hours (ISA, section 5.2). The ISA judged evidence of an association between SO 2 exposure and other health categories to be less convincing; other associations were judged to be suggestive but not sufficient to infer a causal relationship ( i.e., short-term exposure to SO 2 and mortality) or inadequate to infer the presence or absence of a causal relationship ( i.e., short-term exposure to SO 2 and cardiovascular morbidity, and long-term exposure to SO 2 and respiratory morbidity, other morbidity, and mortality). Key conclusions from the ISA are described in greater detail in Table 5-3 of the ISA. As summarized above, the ISA found a “causal” association between short-term (5 minutes to 24 hour) exposure to SO 2 and respiratory morbidity. The evidence leading to this conclusion will be discussed throughout this section as well as in the context of the adequacy of the current and proposed alternative standards (see section II.E and II.F) The ISA also found “suggestive but not sufficient” evidence to infer a causal relationship between short-term SO 2 exposure and mortality. EPA considered this suggestive evidence within the context of proposing a new 1-hour averaging time (see section II.F.2). The association between short- and long-term SO 2 exposure and other health categories was found to be inadequate to infer the presence or absence of a causal relationship and thus, will not be discussed in detail in this notice. Section II.B.1 discusses the results of controlled human exposure studies demonstrating respiratory effects in exercising asthmatics following 5-10 minute exposures to SO 2 , and conclusions in the REA regarding the adversity of such effects. Section II.B.2 discusses the respiratory effects reported in U.S. epidemiologic studies of respiratory symptoms, as well as emergency department visits and hospital admissions for all respiratory causes and asthma. Section II.B.3 discusses ISA conclusions regarding short-term (5 minutes to 24-hours) exposure to SO 2 and respiratory effects, and section II.B.4 discusses long-term SO 2 exposure and potentially adverse health effects. Finally, section II.B.5 discusses SO 2 -related impacts on public health. 1. Respiratory effects and 5-10 minute exposure to SO 2 As noted above, the ISA concluded that there was sufficient evidence to infer a causal relationship between respiratory morbidity and short-term (5-minutes to 24-hours) exposure to SO 2 (ISA, section 5.2). This determination was primarily based on controlled human exposure studies demonstrating a relationship between 5-10 minute peak SO 2 exposures and adverse effects on the respiratory system in exercising asthmatics. The ISA described the controlled human exposure results as being the “definitive evidence” for its causal finding (ISA, section 5.2; p. 5-2). Since the last review, several additional controlled human exposure studies have been published that provide supportive evidence of SO 2 -induced decrements in lung function and increases in respiratory symptoms among exercising asthmatics (see ISA, Annex Table D-2). However, based in part on recent guidance from the American Thoracic Society (ATS) regarding what constitutes an adverse health effect of air pollution (ATS, 2000), a much larger body of key older studies described in the prior review were analyzed in the ISA along with studies published since the last review. In their official statement, the ATS concluded that an air pollution-induced shift in a population distribution of a given health-related endpoint ( e.g., lung function) should be considered adverse, even if this shift does not result in the immediate occurrence of illness in any one individual in the population (ATS 2000). The ATS also recommended that transient loss in lung function with accompanying respiratory symptoms attributable to air pollution should be considered adverse. However, it was noted in the ISA that symptom perception is highly variable among asthmatics even during severe episodes of asthmatic bronchoconstriction, and that an asymptomatic decrease in lung function may pose a significant health risk to asthmatic individuals as it is less likely that these individuals will seek treatment (ISA, section 3.1.3). Therefore, whereas the conclusions in the prior review of the SO 2 NAAQS were based on SO 2 exposure concentrations which resulted in large decrements in lung function and moderate to severe respiratory symptoms, the ISA's current review of data from controlled human exposure studies focused on moderate to large SO 2 -induced decrements in lung function and/or respiratory symptoms ranging from mild (perceptible wheeze or chest tightness) to severe (breathing distress requiring the use of a bronchodilator). See also section II.B.1.c below discussing adversity of effects. Key controlled human exposure studies of respiratory symptoms and lung function are described briefly below and in more detail in section 3.1.3 of the ISA. a. Respiratory symptoms Numerous free-breathing controlled human exposure studies have evaluated respiratory symptoms ( e.g. cough, wheeze, or chest tightness) in exercising asthmatic following 5-10 minute SO 2 exposures. Linn et al. (1983) reported that 5-minute exposures to SO 2 levels as low as 400 ppb resulted in exercising asthmatics experiencing statistically significant increases in respiratory symptoms ( e.g., wheeze, chest tightness, cough, substernal irritation). In a separate study, exercising asthmatics exhibited respiratory symptoms following a 10-minute exposure to 400-600 ppb SO 2 (Linn et al., (1987); Smith (1993)). Gong et al., (1995) exposed SO 2 -sensitive asthmatics to 0, 500 and 1000 ppb SO 2 for 10 minutes while performing different levels of exercise (light, medium, or heavy) and reported that respiratory symptoms increased with increasing SO 2 concentrations. The authors further reported that exposure to 500 ppb SO 2 during light exercise evoked a more severe symptomatic response than heavy exercise in clean air. In addition to these free breathing chamber results described above, studies using mouthpiece exposure systems have reported respiratory symptoms within minutes of SO 2 exposure. 4 Balmes et al. (1987) reported that 7 out of 8 exercising asthmatics developed respiratory symptoms following a 500 ppb 3-minute exposure to SO 2 via mouthpiece (ISA section 3.1.3.1). In an additional study, Trenga et al. (1999) reported increases in respiratory symptoms in exercising asthmatics following 10-minute exposures to 500 ppb SO 2. Although not directly comparable to the free-breathing chamber results described above, these mouthpiece exposure results nonetheless support an association between SO 2 exposure and respiratory symptoms. 4 Studies utilizing a mouthpiece exposure system cannot be directly compared to studies involving freely breathing subjects, as nasal absorption of SO 2 is bypassed during oral breathing, thus allowing a greater fraction of inhaled SO 2 to reach the tracheobronchial airways. As a result, individuals exposed to SO 2 through a mouthpiece are likely to experience greater respiratory effects from a given SO 2 exposure. b. Lung function decrements The ISA found that in free-breathing chamber studies, asthmatic individuals exposed to SO 2 concentrations as low as 200-300 ppb for 5-10 minutes during exercise have been shown to experience moderate or greater bronchoconstriction, measured as a decrease in Forced Expiratory Volume in the first second (FEV 1 ) of ≥ 15%, or an increase in specific airway resistance (sRaw) of ≥ 100% after correction for exercise-induced responses in clean air (Bethel et al., 1985; Linn et al., 1983, 1987; 1988; 1990; Roger et al., 1985). 5 In addition, the ISA concluded that among asthmatics, both the percentage of individuals affected, and the severity of the response increases with increasing SO 2 concentrations. That is, at concentrations ranging from 200-300 ppb, the lowest levels tested in free breathing chamber studies, 6 approximately 5-30% of exercising asthmatics experience moderate or greater decrements in lung function (ISA, Table 3-1). At concentrations of 400-600 ppb, moderate or greater decrements in lung function occur in approximately 20-60% of exercising asthmatics, and compared to exposures at 200-300 ppb, a larger percentage of asthmatics experience severe decrements in lung function ( i.e., ≥ 200% increase in sRaw, and/or a ≥ 20% decrease in FEV 1 ) (ISA, Table 3-1). The ISA also noted that at SO 2 concentrations ≥ 400 ppb, moderate or greater decrements in lung function are frequently accompanied by respiratory symptoms ( e.g., cough, wheeze, chest tightness, shortness of breath) (ISA, Table 3-1). Further analysis and discussion of the individual studies presented above can be found in Sections 3.1.1 to 3.1.3.5 of the ISA. 5 FEV 1 and sRaw are measures of bronchoconstriction. Decreases in FEV 1 or increases in sRaw can result in difficulty breathing. 6 The ISA cites one chamber study with intermittent exercise where healthy and asthmatic children were exposed to 100 ppb SO 2 in a mixture with ozone and sulfuric acid. The ISA notes that compared to exposure to filtered air, exposure to the pollutant mix did not result in statistically significant changes in lung function or respiratory symptoms (ISA section 3.1.3.4) In addition to the evidence from free-breathing chamber studies, the ISA notes very limited evidence of decrements in lung function in exercising asthmatics exposed to lower levels of SO 2 via mouthpiece. That is, the ISA cites two studies where some exercising asthmatics had small changes in FEV 1 or sRaw following exposure to 100 ppb SO 2 via mouthpiece (Koenig et al., 1990 and Sheppard et al., 1981). c. Adversity of 5-10 minute respiratory effects The ATS has previously defined adverse respiratory health effects as “medically significant physiologic changes generally evidenced by one or more of the following: (1) Interference with the normal activity of the affected person or persons, (2) episodic respiratory illness, (3) incapacitating illness, (4) permanent respiratory injury, and/or (5) progressive respiratory dysfunction” (ATS 1985). The ATS has also recommended that transient loss in lung function with accompanying respiratory symptoms, or detectable effects of air pollution on clinical measures ( e.g., medication use) be considered adverse (ATS 1985). In addition, the REA noted that during the last O 3 NAAQS review, the Criteria Document (CD) and Staff Paper indicated that for many people with lung disease ( e.g., asthma), even moderate decrements in lung function ( e.g., FEV 1 decrements > 10% but < 20% and/or ≥ 100% increases in sRaw) or respiratory symptoms would likely interfere with normal activities and result in additional and more frequent use of medication (EPA 2006, EPA 2007d). The REA also noted that CASAC has previously indicated that in the context of standard setting, a focus on the lower end of the range of moderate functional responses is most appropriate for estimating potentially adverse lung function decrements in people with lung disease (73 FR16463). Finally, the REA noted that in the current SO 2 NAAQS review, clinicians on the CASAC Panel again advised that moderate or greater decrements in lung function can be clinically significant in some individuals with respiratory disease (hearing transcripts from USEPA Clean Air Scientific Advisory Committee (CASAC), July 30-31, 2008, Sulfur Oxides-Health Criteria (part 3 of 4) pages 211-213). 7 7 These transcripts can be found in Docket ID No. EPA-HQ-ORD-2006-0260. Available at www.regulations.gov . As previously mentioned, the ATS published updated guidelines on what constitutes an adverse health effect of air pollution in 2000 (ATS, 2000). Among other considerations, the 2000 guidelines stated that measurable negative effects of air pollution on quality of life should be considered adverse (ATS 2000). These updated guidelines also indicated that exposure to air pollution that increases the risk of an adverse effect to the entire population is adverse, even though it may not increase the risk of any individual to an unacceptable level (ATS 2000). For example, a population of asthmatics could have a distribution of lung function such that no individual has a level associated with significant impairment. Exposure to air pollution could shift the distribution to lower levels that still do not bring any individual to a level that is associated with clinically relevant effects. However, this would be considered adverse because individuals within the population would have diminished reserve function, and therefore would be at increased risk if affected by another agent (ATS 2000). At SO 2 concentrations ≥ 400 ppb, controlled human exposure studies have reported decrements in lung function that are often statistically significant at the group mean level, and that are frequently accompanied by respiratory symptoms. Being mindful that the ATS guidelines described above specifically indicate decrements in lung function with accompanying respiratory symptoms as being adverse, exposure to 5-10 minute SO 2 concentrations ≥ 400 ppb are clearly adverse. The ISA has also reported that exposure to SO 2 concentrations as low as 200-300 ppb for 5-10 minutes results in approximately 5-30% of exercising asthmatics experiencing moderate or greater decrements in lung function (defined in terms of a ≥ 15% decline in FEV 1 or 100% increase in sRaw; ISA, Table 3-1). Considering the 2000 ATS guidelines mentioned above, the REA found that these results could reasonably indicate an SO 2 -induced shift in these lung function measurements for this population. As a result, a significant percentage of exercising asthmatics exposed to SO 2 concentrations as low as 200 ppb would have diminished reserve lung function and would be at greater risk if affected by another respiratory agent ( e.g., viral infection). Importantly, diminished reserve lung function in a population that is attributable to air pollution is an adverse effect under ATS guidance. In addition to the 2000 ATS guidelines, the REA was also mindful of: (1) Previous CASAC recommendations (Henderson 2006) and NAAQS review conclusions (EPA 2006, EPA 2007d) indicating that moderate decrements in lung function can be clinically significant in some asthmatics; and (2) subjects participating in these controlled human exposure studies not likely including the most severe asthmatics. Taken together, the REA concluded that exposure to SO 2 concentrations at least as low as 200 ppb can result in adverse health effects in asthmatics. Importantly, the final REA noted that this conclusion was in agreement with CASAC comments following the first draft SO 2 REA (REA section 4.3). The first draft SO 2 REA focused its analyses on exposures and risk associated with 5-minute SO 2 concentrations ≥ 400 ppb. However, CASAC strongly advised the Administrator that effects to exercising asthmatics at levels at least as low as 200 ppb can be adverse, and thus, should be considered in the second draft and final REAs (Henderson 2008). 2. Respiratory effects and 1- to 24-hour exposure to SO 2 In addition to the controlled human exposure evidence described above, the ISA based its causal finding of an association between short-term (5-minutes to 24-hours) exposure to SO 2 and respiratory morbidity on results from epidemiologic studies of respiratory symptoms, as well as ED visits and hospital admissions for all respiratory causes and asthma. More specifically, the ISA describes the results from these epidemiologic studies as providing “supporting evidence” for its determination of causality (ISA section 5.2). Key epidemiologic studies of respiratory symptoms, as well as ED visits and hospital admissions are discussed below. a. Respiratory symptoms The ISA found that the strongest epidemiologic evidence of an association between short-term SO 2 concentrations and respiratory symptoms was in children. Studies conducted in North America and abroad generally reported positive associations between ambient SO 2 concentrations and respiratory symptoms in children. U.S. studies of respiratory symptoms in children (identified from Table 5-4 of the ISA), including three large multi-city studies, are described briefly below and in more detail in section 3.1.4.1 of the ISA. The National Cooperative Inner-City Asthma Study (NCICAS, Mortimer et al. 2002) included asthmatic children (n = 846) from eight U.S. urban areas and examined the relationship between respiratory symptoms and summertime air pollution levels. The strongest associations were found between morning symptoms ( e.g., morning cough) and the median 3-hour average SO 2 concentrations during morning hours (8 a.m. to 11 a.m.)—following a 1- to 2-day lag (ISA, Figure 3-2). Three-hour average concentrations in the morning hours ranged from 17 ppb in Detroit to 37 ppb in East Harlem, NY. This relationship remained robust and statistically significant in multi-pollutant models with ozone (O 3 ), and nitrogen dioxide (NO 2 ). When PM 10 was also added to the model, the effect estimate remained relatively unchanged, although was no longer statistically significant (ISA, Figure 3-2). However, the ISA noted that the loss of statistical significance could have been the result of reduced statistical power since only three of the eight cities were included in the multi-pollutant analysis with PM (ISA, section 3.1.4.1). The Childhood Asthma Management Program (CAMP, Schildcrout et al. 2006) examined the association between ambient air pollution and asthma exacerbations in children (n = 990) from eight North American cities. The median 24-hour average SO 2 concentrations (collected in seven of the eight study locations) ranged from 2.2 ppb in San Diego to 7.4 ppb in St. Louis. Positive associations with an increased risk of asthma symptoms were observed at all lags, but only the association at the 3-day moving average was statistically significant (ISA, Figure 3-3). In joint-pollutant models with carbon monoxide (CO) and NO 2, the 3-day moving average effect estimates remained robust and statistically significant. In a joint-pollutant model with PM 10 , the 3-day moving average effect estimate remained relatively unchanged, but was no longer statistically significant (ISA Figure 3-3). A longitudinal study of schoolchildren (n = 1,844) during the summer months from the Harvard Six Cities Study suggested that the association between SO 2 and respiratory symptoms may potentially be confounded by PM 10 (Schwartz et al., 1994). It should be noted that unlike the NCICAS and CAMP studies, this study was not limited to asthmatic children. The median 24-hour average SO 2 concentration during this period was 4.1 ppb. SO 2 concentrations were found to be statistically significantly associated with cough incidence and lower respiratory symptoms in single pollutant models. However, the effect of SO 2 was substantially reduced and no longer statistically significant after adjustment for PM 10 in a co-pollutant model. The ISA noted that because PM 10 concentrations were correlated strongly to SO 2 -derived sulfate particles (r = 0.80), the reduced SO 2 effect estimate may indicate that for PM 10 dominated by fine sulfate particles, PM 10 has a slightly stronger association than SO 2 to cough incidence and lower respiratory symptoms (ISA, section 3.1.4.1.1). In addition to the three U.S. multi-city studies mentioned above, evidence of an association between ambient SO 2 and respiratory symptoms in children was found in two additional U.S. respiratory symptom studies. Delfino et al., (2003) reported a statistically significant positive association between 1-hour daily maximum SO 2 concentrations in Los Angeles and respiratory symptoms in Hispanic children with asthma (n = 22). Similarly, Neas et al., (1995) reported a positive association between 12-hour average SO 2 concentrations in Uniontown, PA and incidence of evening cough in 4th and 5th graders (n = 83; ISA section 3.1.4.1). Neither of these single city studies employed multi-pollutant models, but given the consistency of results with other epidemiologic evidence, they nonetheless support the association between ambient SO 2 concentrations and respiratory symptoms in children. b. Emergency department visits and hospitalizations Respiratory causes for ED and hospitalization visits typically include asthma, pneumonia, Chronic Obstructive Pulmonary Disorder (COPD), upper and lower respiratory infections, as well as other minor categories. Since the last review, there have been more than 50 peer reviewed epidemiologic studies published worldwide and overall, the ISA concluded that these studies provide evidence to support an association between ambient SO 2 concentrations and ED visits and hospitalizations for all respiratory causes and asthma (ISA, section 3.1.4.6). Notably, the ISA also found that when analyses of ED visit and hospitalizations for all respiratory causes were restricted by age, the results among children (0-14 years) and older adults (65+ years) were mainly positive, but not always statistically significant (ISA, section 3.1.4.6). In these same studies, when all age groups were combined, the ISA found that the results were mainly positive; however, the excess risk estimates were generally smaller compared to children and older adults (ISA, Figure 3-6). Results from key ED visit and hospital admission studies conducted in the U.S. are described in general below, and a more detailed discussion of both the U.S. and international literature can be found in the ISA (ISA, section 3.1.4.6). Of the respiratory ED visit and hospital admission studies reviewed in the ISA, 10 key studies were conducted in the United States (ISA, Table 5-5). Of these 10 studies, three evaluated associations with SO 2 using multi-pollutant models (Schwartz et al., (1995) in Tacoma, WA and New Haven CT; New York Department of Health (NYDOH), (2006) in Bronx and Manhattan, NY; and Ito et al., (2007) in New York City), while seven studies evaluated the SO 2 effect using only single pollutant models (Wilson et al., (2005) in Manchester, NH and Portland, ME; Peel et al., (2005) in Atlanta, GA; Tolbert et al., (2007) in Atlanta GA; Jaffe et al., (2003) in Cleveland, Cincinnati and Columbus, OH; Schwartz et al., (1996) in Cleveland OH; Sheppard et al., (2003) in Seattle, WA; and Lin et al., (2004) in Bronx, NY). Taken together, these studies generally reported positive, but frequently not statistically significant associations between ambient SO 2 and ED visits and hospital admissions for all respiratory causes and for asthma. With regard to U.S. studies employing multi-pollutant models, results reported in Bronx, NY (NYDOH 2006) and New York City, NY (Ito et al., 2007) remained robust and statistically significant in the presence of PM 2.5, [10% (4, 16) and 29.6% (14.3, 46.8), respectively] while in New Haven, CT (Schwartz et al., 1995) results remained robust and statistically significant in the presence of PM 10 [2% (1, 3)]. However, in Manhattan, NY (NYDOH 2006) results reported from single, and multi-pollutant models were negative (although not statistically significantly negative), and in Tacoma, WA (Schwartz et al., 1995) the SO 2 effect estimate [3% (1,6)] was reduced and no longer statistically significant in a multi-pollutant model with PM 10 [−1% (−4, 3)]. In models including gaseous co-pollutants, the SO 2 effect estimate in the Bronx, NY (NYDOH 2006) remained statistically significant in the presence of NO 2 [10% (4,15)], while in NYC (Ito et al., 2007) the SO 2 effect estimate remained statistically significant in the presence of O 3 [26.8% (13.7, 41.5)] and CO [31.1% (16.7, 47.2)], but not in the presence of NO 2 [−1.6% (−16.7, 16.1)]. 3. ISA conclusions regarding short-term (5-minutes to 24-hours) SO 2 exposures As noted above, the ISA found that moderate or greater decrements in lung function occur in some exercising asthmatics exposed to SO 2 concentrations as low as 200-300 ppb for 5-10 minutes. The ISA also found that among asthmatics, both the percentage of individuals affected, and the severity of the response increased with increasing SO 2 concentrations. That is, at 5-10 minute concentrations ranging from 200-300 ppb, the lowest levels tested in free breathing chamber studies, approximately 5-30% percent of exercising asthmatics experienced moderate or greater decrements in lung function (ISA, Table 3-1). At concentrations of 400-600 ppb, moderate or greater decrements in lung function occurred in approximately 20-60% of exercising asthmatics, and compared to exposures at 200-300 ppb, a larger percentage of asthmatics experienced severe decrements in lung function ( i.e., ≥200% increase in sRaw, and/or a ≥20% decrease in FEV 1 ) (ISA, Table 3-1). Moreover, at SO 2 concentrations ≥400 ppb (5-10 minute exposures), moderate or greater decrements in lung function were frequently accompanied by respiratory symptoms. In addition, the ISA concluded that epidemiologic studies of respiratory symptoms in children, as well as emergency department visits and hospitalizations for all respiratory causes and asthma were consistent and coherent. This evidence was consistent in that associations were reported in studies conducted in numerous locations and with a variety of methodological approaches (ISA, section 5.2). It was coherent in that respiratory symptom results from epidemiologic studies of short-term (predominantly 1-hour daily maximum or 24-hour average) SO 2 concentrations were generally in agreement with respiratory symptom results from controlled human exposure studies of 5-10 minutes. These results were also coherent in that the respiratory effects observed in controlled human exposure studies of 5-10 minutes provided a basis for a progression of respiratory morbidity that could lead to the ED visits and hospitalizations observed in epidemiologic studies (ISA, section 5.2). In addition, the ISA concluded that U.S. and international epidemiologic studies employing multi-pollutant models suggested that SO 2 had a generally independent effect on respiratory morbidity outcomes (ISA, section 5.2). The ISA also found that the respiratory effects of SO 2 were consistent with the mode of action as it is currently understood from animal toxicological and human exposure studies (ISA, section 5.2). The immediate effect of SO 2 on the respiratory system is bronchoconstriction. This response is mediated by chemosensitive receptors in the tracheobronchial tree. Activation of these receptors triggers central nervous system reflexes that result in bronchoconstriction and respiratory symptoms that are often followed by rapid shallow breathing (ISA, section 5.2). The ISA noted that asthmatics are likely more sensitive to the respiratory effects of SO 2 due to pre-existing inflammation associated with the disease. For example, pre-existing inflammation may lead to enhanced release of inflammatory mediators, and/or enhanced sensitization of the chemosensitive receptors (ISA, section 5.2). Taken together, the ISA concluded that the controlled human exposure, epidemiologic, and toxicological evidence supported its determination of a causal relationship between respiratory morbidity and short-term (5-minutes to 24-hours) exposure to SO 2 . 4. Health effects and long-term exposures to SO 2 There were numerous studies published since the last review examining possible associations between long-term SO 2 exposure and mortality and morbidity (respiratory morbidity, carcinogenesis, adverse prenatal and neonatal outcomes) endpoints. However, the ISA concluded that the evidence relating long-term (weeks to years) SO 2 exposure to adverse health effects was “inadequate to infer the presence or absence of a causal relationship” (ISA, Table 5-3). That is, the ISA found the long-term health evidence to be of insufficient quantity, quality, consistency, or statistical power to make a determination as to whether SO 2 was truly associated with these health outcomes (ISA, Table 1-2). 5. SO 2 -related impacts on public health Interindividual variation in human responses to air pollutants indicates that some subpopulations are at increased risk for the detrimental effects of ambient exposure to SO 2 . The NAAQS are intended to provide an adequate margin of safety for both general populations and sensitive subpopulations, or those subgroups potentially at increased risk for health effects in response to ambient air pollution. To facilitate the identification of subpopulations at the greatest risk for SO 2 -related health effects, studies have identified factors that contribute to the susceptibility and/or vulnerability of an individual to SO 2 . Susceptible individuals are broadly defined as those with a greater likelihood of an adverse outcome given a specific exposure in comparison with the general population (American Lung Association, 2001). The susceptibility of an individual to SO 2 can encompass a multitude of factors which represent normal developmental phases ( e.g., age) or biologic attributes ( e.g., gender); however, other factors ( e.g., socioeconomic status (SES)) may influence the manifestation of disease and also increase an individual's susceptibility (American Lung Association, 2001). In addition, subpopulations may be vulnerable to SO 2 in response to an increase in their exposure during certain windows of life ( e.g., childhood or old age) or as a result of external factors ( e.g., SES) that contribute to an individual being disproportionately exposed to higher concentrations than the general population. It should be noted that in some cases specific factors may affect both the susceptibility and vulnerability of a subpopulation to SO 2 . For example, a subpopulation that is characterized as having low SES may have less access to healthcare resulting in the manifestation of a disease, which increases their susceptibility to SO 2 , but they may also reside in a location that results in exposure to higher concentrations of SO 2 , increasing their vulnerability to SO 2 . To examine whether SO 2 differentially affects certain subpopulations, stratified analyses are often conducted in epidemiologic investigations to identify the presence or absence of effect modification. A thorough evaluation of potential effect modifiers may help identify subpopulations that are more susceptible and/or vulnerable to SO 2 . These analyses require the proper identification of confounders and their subsequent adjustment in statistical models, which helps separate a spurious from a true causal association. Although the design of toxicological and human clinical studies does not allow for an extensive examination of effect modifiers, the use of animal models of disease and the study of individuals with underlying disease or genetic polymorphisms do allow for comparisons between subgroups. Therefore, the results from these studies, combined with those results obtained through stratified analyses in epidemiologic studies, contribute to the overall weight of evidence for the increased susceptibility and vulnerability of specific subpopulations to SO 2 . Those groups identified in the ISA to be potentially at greater risk of experiencing an adverse health effect from SO 2 exposure are described in more detail below. a. Pre-existing respiratory disease In human clinical studies, asthmatics have been shown to be more responsive to the respiratory effects of SO 2 exposure than healthy non-asthmatics. Although SO 2 -attributable decrements in lung function have generally not been demonstrated at concentrations ≤ 1000 ppb in non-asthmatics, statistically significant increases in respiratory symptoms and decreases in lung function have consistently been observed in exercising asthmatics following 5-10 minute SO 2 exposures at concentrations ranging from 400-600 ppb (ISA, section 4.2.1.1). Moderate or greater SO 2 -induced decrements in lung function have also consistently been observed at SO 2 concentrations ranging from 200-300 ppb in some asthmatics. The ISA also noted that a number of epidemiologic studies have reported respiratory morbidity in asthmatics associated with ambient SO 2 concentrations (ISA 4.2.1.1). For example, numerous epidemiologic studies have observed positive associations between ambient SO 2 concentrations and ED visits and hospitalizations for asthma (ISA section 4.2.1.1). Overall, the ISA concluded that epidemiologic and controlled human exposure studies indicated that individuals with pre-existing respiratory diseases, particularly asthma, are at greater risk than the general population of experiencing SO 2 -associated health effects (ISA, section 4.2.1.1). b. Genetics The ISA noted that a consensus now exists among scientists that the potential for genetic factors to increase the risk of experiencing adverse health effects due to ambient air pollution merits serious consideration. Several criteria must be satisfied in selecting and establishing useful links between polymorphisms in candidate genes and adverse respiratory effects. First, the product of the candidate gene must be significantly involved in the pathogenesis of the effect of interest, which is often a complex trait with many determinants. Second, polymorphisms in the gene must produce a functional change in either the protein product or in the level of expression of the protein. Third, in epidemiologic studies, the issue of effect modification by other genes or environmental exposures must be carefully considered (ISA section 4.2.2). Although many studies have examined the association between genetic polymorphisms and susceptibility to air pollution in general, only one study has specifically examined the effects of SO 2 exposure on genetically distinct subpopulations. Winterton et al. (2001) found a significant association between SO 2 -induced decrements in FEV 1 and the homozygous wild-type allele in the promoter region of Tumor Necrosis Factor-α (TNF- α; AA, position-308). However, the ISA concluded that the overall body of evidence was too limited to reach a conclusion regarding the effects of SO 2 exposure on genetically distinct subpopulations at this time. c. Age The ISA identified children ( i.e., < 18 years of age) and older adults ( i.e., > 65 years of age) as groups that are potentially at greater risk of experiencing SO 2 -associated adverse health effects. In children, the developing lung is prone to damage from environmental toxicants as it continues to develop through adolescence. The biological basis for increased risk in the elderly is unknown, but one hypothesis is that it may be related to changes in antioxidant defenses in the fluid lining the respiratory tract. The ISA found a number of epidemiologic studies that observed increased respiratory symptoms in children associated with increasing SO 2 concentrations. In addition, several studies have reported that the excess risk estimates for ED visits and hospitalizations for all respiratory causes, and to a lesser extent asthma, associated with a 10-ppb increase in 24-hour average SO 2 concentrations were higher for children and older adults than for all ages together (ISA, section 4.2.3). However, the ISA also noted that the evidence from controlled human exposure studies does not suggest that adolescents are either more or less at risk than adults to the respiratory effects of SO 2 , but rather adolescents may experience similar respiratory effects at a given exposure concentration (ISA, sections 3.1.3.5 and 4.2.3). 8 Overall, the ISA found that compared to the general population, there was limited evidence to suggest that children and older adults are at greater risk of experiencing SO 2 -associated health effects (ISA, section 4.2.3). 8 Very young children are not included in controlled human exposure studies and this absence of data on what is likely to be a sensitive life stage is a source of uncertainty for children's susceptibility. d. Time spent outdoors Outdoor SO 2 concentrations are generally much higher than indoor concentrations. Thus, the ISA noted that individuals who spend a significant amount of time outdoors are likely at greater risk of experiencing SO 2 -associated health effects than those who spend most of their time indoors (ISA section 4.2.5). e. Ventilation rate Controlled human exposure studies have demonstrated that decrements in lung function and respiratory symptoms occur at significantly lower SO 2 exposure levels in exercising subjects compared to resting subjects. As ventilation rate increases, breathing shifts from nasal to oronasal, thus resulting in greater uptake of SO 2 in the tracheobronchial airways due to the diminished absorption of SO 2 in the nasal passages. Therefore, individuals who spend a significant amount of time at elevated ventilation rates ( e.g. while playing, exercising, or working) are expected to be at greater risk of experiencing SO 2 -associated health effects (ISA section 4.2.5). f. Socioeconomic status There is limited evidence that increased risk to SO 2 exposure is associated with lower SES (ISA section 4.2.5). Finkelstein et al. (2003) found that among people with below-median income, the relative risk for above-median exposure to SO 2 was 1.18 (95% CI: 1.11, 1.26); the corresponding relative risk among subjects with above-median income was 1.03 (95% CI: 0.83, 1.28). However, the ISA concluded that there was insufficient evidence to reach a conclusion regarding SES and exposure to SO 2 at this time (ISA section 4.2.5). g. Size of at-risk populations Considering the size of the groups mentioned above, large proportions of the U.S. population are likely to have a relatively high risk of experiencing SO 2 -related health effects. In the United States, approximately 7% of adults and 9% of children have been diagnosed with asthma. Notably, the prevalence and severity of asthma is higher among certain ethnic or racial groups such as Puerto Ricans, American Indians, Alaskan Natives, and African Americans (EPA 2008b). Furthermore, a higher prevalence of asthma among persons of lower SES and an excess burden of asthma hospitalizations and mortality in minority and inner-city communities have been observed. In addition, population groups based on age comprise substantial segments of individuals that may be potentially at risk for SO 2 -related health impacts. Based on U.S. census data from 2000, about 72.3 million (26%) of the U.S. population are under 18 years of age, 18.3 million (7.4%) are under 5 years of age, and 35 million (12%) are 65 years of age or older. There is also concern for the large segment of the population that is potentially at risk to SO 2 -related health effects because of increased time spent outdoors at elevated ventilation rates (those who work or play outdoors). Overall, the considerable size of the population groups at risk indicates that exposure to ambient SO 2 could have a significant impact on public health in the United States. C. Human exposure and health risk characterization To put judgments about SO 2 -associated health effects into a broader public health context, EPA has drawn upon the results of the quantitative exposure and risk assessments. Judgments reflecting the nature of the evidence and the overall weight of the evidence are taken into consideration in these quantitative exposure and risk assessments, discussed below. These assessments provide estimates of the likelihood that asthmatics at moderate or greater exertion ( e.g. while exercising) would experience SO 2 exposures of potential concern as well as an estimate of the number and percent of exposed asthmatic individuals likely to experience SO 2 -induced lung function responses ( i.e., moderate or greater decrements in lung function defined in terms of sRaw or FEV 1 ) under varying air quality scenarios ( e.g., just meeting the current or alternative standards). These assessments also characterize the kind and degree of uncertainties inherent in such estimates. This section describes the approach taken in the REA to characterize SO 2 -related exposures and health risks. Goals of the REA included estimating short-term exposures and potential human health risks associated with (1) recent levels of ambient SO 2 ; (2) SO 2 levels adjusted to simulate just meeting the current standards; and (3) SO 2 levels adjusted to simulate just meeting potential alternative 1-hour standards. This section discusses the scientific evidence from the ISA that was used as the basis for the risk characterization (II.C.1), the approaches used in characterizing exposures and risks (II.C.2), and important uncertainties associated with these analyses (II.C.3). The results of the exposure and risk analyses, as they relate to the current and potential alternative standards, are discussed in subsequent sections of this proposal (sections II.E and II.F, respectively). 1. Evidence base for the risk characterization As previously mentioned, the ISA concluded that the evidence for an association between respiratory morbidity and SO 2 exposure was “sufficient to infer a causal relationship” (ISA, section 5.2) and that the “definitive evidence” for this conclusion was from the results of 5-10 minute controlled human exposure studies demonstrating decrements in lung function and/or respiratory symptoms in exercising asthmatics (ISA, section 5.2). Accordingly, the REA concluded that quantitative exposure and risk analyses should focus on 5-minute levels of SO 2 in excess of potential health effect benchmark values derived from the controlled human exposure literature (REA, section 6.2). These benchmark levels are not potential standards, but rather are concentrations which represent “exposures of potential concern” which are used in the analyses to estimate potential exposures and risks associated with 5-minute concentrations of SO 2. In addition, although the REA concluded that the epidemiologic evidence was not appropriate for use in quantitative risk analyses (REA, section 6.3), these studies were considered in the selection of potential alternative standards for use in the air quality, exposure and risk analyses (REA, chapter 5), as well as in the REA's assessment of the adequacy of the current and potential alternative primary standards (REA, sections 10.3; 10.4; and 10.5). As mentioned above, the health effect benchmark values used in the REA were derived primarily from the ISA's evaluation of the 5-10 minute controlled human exposure literature. The ISA concluded that moderate or greater decrements in lung function occurred in approximately 5-30% of exercising asthmatics following exposure to 200-300 ppb SO 2 for 5-10 minutes. As explained in section II.B.1.b, the ISA concluded that moderate or greater decrements in lung function occurred in approximately 20-60% of exercising asthmatics following exposure to 400-600 ppb SO 2 for 5-10 minutes. The ISA also concluded that at SO 2 concentrations ≥ 400 ppb, statistically significant moderate or greater decrements in lung function at the group mean level have often been reported and are frequently accompanied by respiratory symptoms (ISA, section 3.1.3.5). In addition to the health evidence from the ISA presented above, when considering potential health effect benchmark levels, the REA noted: (1) Subjects participating in human exposure studies typically do not include individuals who may be most susceptible to the respiratory effects of SO 2, ( e.g., the most severe asthmatics given the obvious ethical issues of subjecting such persons to the clinical tests) and (2) given that approximately 5-30% of exercising asthmatics experienced moderate or greater decrements in lung function following exposure to 200-300 ppb SO 2 (the lowest levels tested in free-breathing chamber studies), it is likely that a percentage of exercising asthmatics would also experience similar decrements in lung function following exposure to levels lower than 200 ppb (REA, section 6.2). That is, the REA concluded that there was no evidence to suggest that 200 ppb represented a threshold level below which no adverse respiratory effects would occur (REA, section 6.2). Moreover, the REA considered that small SO 2 -induced lung function decrements have been observed in exercising asthmatics at concentrations as low as 100 ppb when SO 2 is administered via mouthpiece (ISA, section 3.1.3). Taken together, the REA concluded it appropriate to examine potential 5-minute benchmark values in the range of 100-400 ppb (REA, section 6.2). The lower end of the range considered the factors mentioned above, while the upper end of the range recognized that 400 ppb represents the lowest concentration at which moderate or greater decrements in lung function are frequently accompanied by respiratory symptoms (REA, section 6.2): a combination of effects which would clearly be considered adverse under ATS guidelines (ATS, 1985). Although the analysis of exposures of potential concern were conducted using discrete benchmark levels ( i.e., 100, 200, 300, 400 ppb), EPA recognizes that there is no sharp breakpoint within the continuum ranging from at and above 400 ppb down to 100 ppb. In considering the concept of exposures of potential concern, it is important to balance concerns about the potential for health effects and their severity with the increasing uncertainty associated with our understanding of the likelihood of such effects at lower SO 2 levels. Within the context of this continuum, estimates of exposures of potential concern at discrete benchmark levels provide some perspective on the potential public health impacts of SO 2 -related health effects that have been demonstrated in controlled human exposure studies. They also help in understanding the extent to which such impacts could change by just meeting the current and potential alternative standards. However, estimates of the number of asthmatics likely to experience exposures of potential concern cannot be translated directly into quantitative estimates of the number of people likely to experience specific health effects. Due to individual variability in responsiveness, only a subset of asthmatics exposed at and above a specific benchmark level can be expected to experience health effects. The amount of weight to place on the estimates of exposures of potential concern at any of these benchmark levels depends in part on the weight of the scientific evidence concerning health effects associated with SO 2 exposures at and above that benchmark level. Such public health policy judgments are embodied in the NAAQS standard setting criteria ( i.e., standards that, in the judgment of the Administrator, are requisite to protect public health with an adequate margin of safety). Since exposures of potential concern cannot be directly translated into quantitative estimates of the number of individuals likely to experience specific health effects, the REA not only characterizes exposure and risks utilizing exposures of potential concern, but also uses information from the controlled human exposure literature to conduct a quantitative risk assessment. The quantitative risk assessment estimated the number and percentage of exposed asthmatics at moderate or greater exertion expected to experience a moderate or greater lung function response (in terms of a ≥ 100% increase in sRaw and/or a ≥ 15% decline in FEV 1 ; see section II.C.2). 2. Overview of approaches As noted above, the purpose of the assessments described in the REA was to characterize air quality, exposures, and health risks associated with recent ambient levels of SO 2 , with SO 2 levels that could be associated with just meeting the current SO 2 NAAQS, and with SO 2 levels that could be associated with just meeting potential alternative standards. The REA utilizes three approaches to characterize health risks In the first approach, for each air quality scenario, statistically estimated 9 and measured ambient 5-minute SO 2 concentrations were compared to the 5-minute potential health effect benchmark levels discussed above which (as noted) were derived from the controlled human exposure literature (REA, chapter 7). In the second approach, modeled estimates of 5-minute exposures in asthmatics at moderate or greater exertion ( e.g. while exercising) were compared to these 5-minute potential health effect benchmark levels. In the third approach, exposure-response relationships from individual level data from controlled human exposure studies were used in conjunction with the outputs of the exposure analysis to estimate health impacts under the air quality scenarios mentioned above. A brief description of these approaches is provided below and each approach is described in detail in chapters 7 through 9 of the REA. 9 Benchmark values derived from the controlled human exposure literature were associated with a 5-minute averaging time. However, only 98 ambient monitors located in 13 states from 1997-2007 reported measured 5-minute SO 2 concentrations since such monitoring is not required (see section III). In contrast, 809 monitors in 48 states, DC, Puerto Rico, and the Virgin Islands reported 1-hour SO 2 concentrations over a similar time period. Therefore, to broaden analyses to areas where measured 5-minute SO 2 concentrations were not available, the REA utilized a statistical relationship to estimate the highest 5-minute level in an hour, given a reported 1-hour average SO 2 concentration (REA, section 6.4). Then, similar to measured 5-minute SO 2 levels, statistically estimated 5-minute SO 2 concentrations were compared to 5-minute potential health effect benchmark values. In the first approach, statistically estimated and actual measured 5-minute ambient SO 2 concentrations were compared to 5-minute potential health effect benchmark levels (REA, chapter 7). The results generated from the air quality analysis were considered a broad characterization of national air quality and human exposures that might be associated with these 5-minute SO 2 concentrations. An advantage of the air quality analysis is its relative simplicity; however, there is uncertainty associated with the assumption that SO 2 air quality can serve as an adequate surrogate for total exposure to ambient SO 2 . Actual exposures might be influenced by factors not considered by this approach, including small scale spatial variability in ambient SO 2 concentrations (which might not be captured by the network of fixed-site ambient monitors) and spatial/temporal variability in human activity patterns. In the second approach, an inhalation exposure model was used to generate more realistic estimates of personal exposures in asthmatics (REA, chapter 8). This analysis estimated temporally and spatially variable ambient 5-minute SO 2 concentrations and simulated asthmatics contact with these pollutant concentrations while at moderate or greater exertion ( i.e., while at elevated ventilation rates). The approach was designed to estimate exposures that are not necessarily represented by the existing ambient monitoring data. AERMOD, an EPA dispersion model, was used to estimate 1-hour ambient SO 2 concentrations using emissions estimates from stationary, non-point, and port sources. The Air Pollutants Exposure (APEX) model, an EPA human exposure model, was then used to estimate population exposures using the estimated hourly census block level SO 2 concentrations. From these 1-hour census block concentrations, 5-minute maximum SO 2 concentrations within each hour were estimated using the statistical relationship mentioned above. A probabilistic approach was then used to model asthmatics' exposures considering: (1) Time spent in different microenvironments; (2) time spent at moderate or greater exertion; and (3) the variable SO 2 concentrations that occur within these microenvironments across time, space, and microenvironment type. Estimates of personal exposure to 5-minute SO 2 levels were then compared to the 5-minute potential health benchmark levels ( i.e., 5-minute benchmark levels of 100, 200, 300, and 400 ppb). This approach to assessing exposures was more resource intensive than using ambient levels as an indicator of exposure; therefore, the final REA included the analysis of two locations: St Louis and Greene County, MO. Although the geographic scope of this analysis was limited, the approach provided estimates of SO 2 exposures in asthmatics and asthmatic children in St. Louis and Greene Counties and thus, served to complement the broader air quality characterization. For the characterization of risks in both the air quality analysis and the exposure modeling analysis described above, the REA used a range of 5-minute potential health effect benchmarks: 100, 200, 300, and 400 ppb. These benchmark values were compared to both SO 2 air quality levels and to estimates of SO 2 exposure in asthmatics. When SO 2 air quality was used as an indicator of exposure, a key output of the analysis was an estimate of the number of days per year specific locations experienced statistically estimated 5-minute daily maximum levels of SO 2 that exceeded one of these 5-minute potential health effect benchmarks. When personal exposures were simulated, the output of the analysis was an estimate of the number and percent of asthmatics and asthmatic children at risk for experiencing, at least once per year, a statistically estimated 5-minute daily maximum level of SO 2 of ambient origin in excess of one of these benchmarks. An advantage of using the benchmark approach to characterize health risks is that the effects observed in the controlled human exposure studies clearly result from SO 2 exposure, so the benchmarks are reliable levels at which effects to asthmatics from exposure to SO 2 can occur. A limitation of this approach is that the magnitude of the SO 2 effect on decrements in lung function and respiratory symptoms can vary considerably from individual to individual and thus, not all asthmatics would be expected to respond to the same levels of SO 2 exposure. Therefore, numbers of exposures can be quantified more readily than the number of individuals experiencing SO 2 -induced lung function decrements and/or respiratory symptoms. The third approach was a quantitative risk assessment. This approach combined results from the exposure analysis ( i.e., the number of exposed total asthmatics or asthmatic children while at moderate or greater exertion) with exposure-response functions derived from individual level data from controlled human exposure studies (see ISA, Table 3-1 and Johns (2009) 10 ) to estimate the percentage and number of exposed asthmatics and asthmatic children likely to experience a moderate or greater lung function response ( i.e., decrements in lung function defined in terms of FEV 1 and sRaw) under the air quality scenarios mentioned above (REA, chapter 9). The advantage of this approach is that it recognizes that not all exposed asthmatics at moderate or greater exertion will have a lung function response. Moreover, it is advantageous in that rather than considering discrete potential health effect benchmark levels, it quantitatively estimates the number and percent of asthmatics and asthmatic children likely to experience a moderate or greater lung function response considering the entire distribution of personal exposures. 10 EPA recently conducted a complete quality assurance review of all individual subject data. The results of this review did not substantively change any of the entries in ISA, Table 3-1, and did not in anyway affect the conclusions of the ISA (see Johns and Simmons, 2009). 3. Key limitations and uncertainties The way in which air quality, exposure, and risk results will inform ultimate decisions regarding the current and potential alternative SO 2 standards will depend upon the weight placed on each of the analyses when uncertainties associated with those analyses are taken into consideration. Sources of uncertainty associated with each of the analyses (air quality, exposure, and quantitative risk) are briefly presented below and are described in more detail in chapters 7-9 of the REA. In the air quality analysis, the REA used ambient SO 2 data from both the limited number of monitors reporting 5-minute concentrations and the broader network of monitors reporting 1-hour concentrations of SO 2 to characterize U.S. air quality. There was general agreement in the monitor site attributes and emissions sources potentially influencing ambient monitoring concentrations for each set of data analyzed. However, the REA noted that the greatest relative uncertainty was in the spatial representativeness of both the overall monitoring network and the subsets of monitors chosen for detailed analyses (REA, section 7.4.2.4). An additional source of uncertainty in the air quality analysis is associated with the statistical model used to estimate 5-minute maximum SO 2 concentrations at monitors that reported only 1-hour SO 2 concentrations (REA, section 7.4.2.6). Cross-validation of statistically estimated 5-minute concentrations with the limited number of reported 5-minute SO 2 measurements indicated that the greatest difference in the predicted versus observed numbers of benchmark exceedances occurred at the lower and upper tails of the distribution. However, the REA noted that overall, the results of the cross-validation analysis indicated reasonable model performance (REA, sections 10.3.3.1 and 10.5.2). The air quality characterization assumes that the ambient monitoring data and the estimated days per year with exceedances of the specified benchmark levels can serve as an indicator of exposure. Longer-term personal SO 2 exposure ( i.e., days to weeks) concentrations are correlated with and are a fraction of ambient SO 2 concentrations. However, uncertainty remains in this relationship when considering short-term ( i.e., 5-minute) averaging times because of the lack of comparable measurement data (REA, section 7.4.2.7). The St. Louis and Greene county exposure assessments were also associated with a number of key uncertainties that should be considered when interpreting the results with regard to decisions on the standard. Such uncertainties are highlighted below, and these, as well as other sources of uncertainty, are also discussed in greater depth in section 8.11 of the REA. In the exposure analyses, it was necessary to derive an area source emission profile rather than use a default profile to improve the agreement between ambient measurements and model predicted 1-hour SO 2 concentrations. The improved model performance reduces uncertainty in the 1-hour SO 2 concentrations predictions, but nonetheless remains as an important uncertainty in the absence of actual local source emission profiles (REA, section 8.11.2). The St. Louis and Greene county exposure assessments were performed to better reflect both the temporal and spatial representation of ambient concentrations and to estimate the rate of contact of asthmatic individuals with 5-minute SO 2 concentrations while engaged in moderate or greater exertion. Estimated annual average SO 2 exposures in the two exposure modeling domains are consistent with long-term personal exposures ( i.e., days to weeks) measured in other U.S. locations (REA, chapter 8). However, uncertainty remains in the estimated number of persons with 5-minute SO 2 concentrations above benchmark levels because of the lack of comparable measurement data, particularly considering both the short-term averaging time and geographic location (REA, section 8.11.2). In addition, although all 5-minute ambient SO 2 concentrations in the exposure analyses were estimated by the exposure model, each hour was comprised of the maximum 5-minute SO 2 concentration and eleven other 5-minute SO 2 concentrations normalized to the 1-hour mean concentration. The REA assumed that this approach would reasonably estimate the number of individuals exposed to peak concentrations. Sensitivity analyses revealed that both the number of persons exposed and where peak exposures occur can vary when considering an actual 5-minute temporal profile (REA, Section 8.11.2) A number of key uncertainties should also be considered when interpreting the results of the St. Louis and Greene County risk assessment with regard to decisions on the standard. Such uncertainties associated with the St Louis and Greene County risk assessment are discussed briefly below and in greater depth in section 9.4 of the REA. In the quantitative risk assessment, it was necessary to estimate responses at SO 2 levels below the lowest exposure levels used in the free-breathing controlled human exposure studies ( i.e., below 200 ppb). Probabilistic exposure-response relationships were derived in the REA using two different functional forms ( i.e., probit and 2-parameter logistic), but nonetheless there remains greater uncertainty in responses below 200 ppb because of the lack of comparable experimental data. Moreover, because the controlled human exposure studies used in the risk assessment involved only SO 2 exposures, it was assumed in the REA that estimates of SO 2 -induced health responses are not affected by the presence of other pollutants ( e.g., PM 2.5 , O 3 , NO 2 ; REA, section 9.4). The risk assessment assumes that the SO 2 -induced responses for individuals are reproducible. The REA noted that this assumption had some support in that one study (Linn et al., 1987) exposed the same subjects on two occasions to 600 ppb and the authors reported a high degree of correlation while observing a much lower correlation for the lung function response observed in the clean air with exercise exposure (REA, section 9.4). Because the vast majority of controlled human exposure studies investigating lung function responses were conducted with adult subjects, the risk assessment relies on data from adult asthmatic subjects to estimate exposure-response relationships that have been applied to all asthmatic individuals, including children. The ISA (section 3.1.3.5) indicates that there is a strong body of evidence that suggests adolescents may experience many of the same respiratory effects at similar SO 2 levels, but recognizes that these studies administered SO 2 via inhalation through a mouthpiece (which can result in an increase in lung SO 2 uptake) rather than in an exposure chamber. Therefore, the uncertainty is greater in the risk estimates for asthmatic children (REA, section 9.4) 11 . 11 Very young children were not included in the controlled human exposure data which served as the basis for the exposure-response relationships used in the risk assessment. This absence of data on what is likely to be a sensitive life stage is an additional source of uncertainty in the risk assessment. D. Considerations in review of the standards This section presents the integrative synthesis of the evidence and information contained in the ISA and the REA with regard to the current and potential alternative standards. EPA notes that the final decision on retaining or revising the current primary SO 2 standards is a public health policy judgment to be made by the Administrator. The Administrator's final decision will draw upon scientific information and analyses related to health effects, population exposures, and risks; as well as judgments about the appropriate response to the range of uncertainties that are inherent in the scientific evidence and analyses; and comments received in response to this proposal. 1. Background on the current standards There are currently two SO 2 primary standards. The 24-hour average standard is 0.14 ppm not to be exceeded more than once per year and the annual average standard is 0.03 ppm. In the last review of the SO 2 NAAQS, both the 24-hour and annual standards were retained. The rationale for the retention of these standards is discussed briefly below. In the last review, retention of the 24-hour standard was based largely on epidemiologic studies conducted in London in the 1950s and 1960s. The results of those studies suggested an association between 24-hour average levels of SO 2 and increased daily mortality and aggravation of bronchitis when in the presence of elevated levels of PM (53 FR 14927). Additional epidemiologic evidence suggested that elevated SO 2 levels were associated with the possibility of small, reversible declines in children's lung function (53 FR 14927). However, it was noted that in the locations where these epidemiologic studies were conducted, high SO 2 levels were usually accompanied by high levels of PM, thus making it difficult to disentangle the individual contribution each pollutant had on these health outcomes. It was also noted that rather than 24-hour average SO 2 levels, the health effects observed in these studies may have been related, at least in part, to the occurrence of shorter-term peaks of SO 2 within a 24-hour period (53 FR 14927). Retention of the annual standard in the last review was largely based on an assessment of qualitative evidence gathered from a limited number of epidemiologic studies. The strongest evidence for an association between annual SO 2 concentrations and adverse health effects in the 1982 AQCD was from a study conducted by Lunn et al (1967). The authors found that among children, a likely association existed between chronic upper and lower respiratory tract illnesses and annual SO 2 levels of 70-100 ppb in the presence of 230-301 µg/m 3 black smoke. Three additional studies described in the 1986 Second Addendum also suggested that long-term exposure to SO 2 was associated with adverse respiratory effects. Notably, studies conducted by Chapman et al. (1985) and Dodge et al. (1985) found associations between long-term SO 2 concentrations (with or without high particle concentrations) and cough in children and young adults. However, it was noted that there was considerable uncertainty associated with these studies because they were conducted in locations subject to high, short-term peak SO 2 concentrations ( i.e., locations near point sources); therefore it was difficult to discern whether this increase in cough was the result of long-term, low level SO 2 exposure, or repeated short-term peak SO 2 exposures. It was concluded in the last review that there was no quantitative rationale to support a specific range for an annual standard (EPA, 1994b). However, it was also found that although no single epidemiologic study provided clear quantitative conclusions, there appeared to be some consistency across studies indicating the possibility of respiratory effects associated with long-term exposure to SO 2 just above the level of the existing annual standard (EPA, 1994b). In addition, air quality analyses conducted during the last review indicated that the short-term standards being considered (1-hour and/or 24-hour) could not by themselves prevent long-term concentrations of SO 2 from exceeding the level of the existing annual standard in several large urban areas. Ultimately, both the scientific evidence and the air quality analyses were used by the Administrator to conclude that retaining the existing annual standard was requisite to protect human health. 12 12 Section I.C above discusses potential standards considered but not adopted in the last review, notably some type of standard to deal with effects of 5 to 10 minute exposures. 2. Approach for reviewing the need to retain or revise the current standards The decision in the present review on whether the current 24-hour and/or annual standards are requisite to protect public health with an adequate margin of safety will be informed by a number of scientific studies and analyses that were not available in the 1996 review. Specifically, as discussed above (section II.B), a large number of epidemiologic studies have been published since the 1996 review. Many of these studies evaluated associations between SO 2 and adverse respiratory endpoints ( e.g., respiratory symptoms, emergency department visits, hospital admissions) in locations where 24-hour and annual average SO 2 concentrations were below the levels allowed by the current standards. In addition, with respect to adverse health effects associated with 5-minute SO 2 concentrations, the REA described estimates of SO 2 -associated health risks that could be present in counties that just meet the current 24-hour or annual standards, whichever was controlling in a given county. 13 The approach for considering this scientific evidence and exposure/risk information is discussed below. 13 As noted in the REA, the controlling standard by definition would be the standard that allows air quality to just meet either the annual concentration level of 30.4 ppb ( i.e., the annual standard is the controlling standard) or the 2nd highest 24-hour concentration level of 144 ppb ( i.e., the 24-hour standard is the controlling standard). The factor selected is derived from a single monitor within each county (even if there is more than one monitor in the county) for a given year. A different (or the same) monitor in each county could be used to derive the factor for other years; the only requirement for selection is that it be the lowest factor, whether derived from the annual or 24-hour standard level. To evaluate whether the current primary SO 2 standards are adequate or whether consideration of revisions is appropriate, EPA is using an approach in this review described in chapter 10 of the REA which builds upon the approaches used in reviews of other criteria pollutants, including the most recent reviews of the NO 2 , Pb, O 3 , and PM NAAQS (EPA, 2008c; EPA, 2007c; EPA, 2007d; EPA, 2005), and reflects the body of evidence and information that is currently available. As in other recent reviews, EPA's considerations will include the implications of placing more or less weight or emphasis on different aspects of the scientific evidence and the exposure/risk-based information, recognizing that the weight to be given to various elements of the evidence and exposure/risk information is part of the public health policy judgments that the Administrator will make in reaching decisions on the standard. A series of general questions frames this approach to considering the scientific evidence and exposure-/risk-based information. First, EPA's consideration of the scientific evidence and exposure/risk information with regard to the adequacy of the current standards is framed by the following questions: • To what extent does evidence that has become available since the last review reinforce or call into question evidence for SO 2 -associated effects that were identified in the last review? • To what extent has evidence for different health effects and/or sensitive populations become available since the last review? • To what extent have uncertainties identified in the last review been reduced and/or have new uncertainties emerged? • To what extent does evidence and exposure-/risk-based information that has become available since the last review reinforce or call into question any of the basic elements of the current standard? To the extent that the available evidence and exposure-/risk-based information suggests it may be appropriate to consider revision of the current standards, EPA considers that evidence and information with regard to its support for consideration of a standard that is either more or less stringent than the current standards. This evaluation is framed by the following questions: • Is there evidence that associations, especially causal or likely causal associations, extend to ambient SO 2 concentrations as low as, or lower than, the concentrations that have previously been associated with health effects? If so, what are the important uncertainties associated with that evidence? • Are exposures above benchmark levels and/or health risks estimated to occur in areas that meet the current standard? If so, are the estimated exposures and health risks important from a public health perspective? What are the important uncertainties associated with the estimated risks? To the extent that there is support for consideration of a revised standard, EPA then considers the specific elements of the standard (indicator, averaging time, form, and level) within the context of the currently available information. In so doing, the Agency addresses the following questions regarding the elements of the standard: • Does the evidence provide support for considering a different indicator for gaseous SO X ? • Does the evidence provide support for considering different, or additional averaging times? • What ranges of levels and forms of alternative standards are supported by the evidence, and what are the associated uncertainties and limitations? • To what extent do specific averaging times, levels, and forms of alternative standards reduce the estimated exposures above benchmark levels and risks attributable to exposure to ambient SO 2 , and what are the uncertainties associated with the estimated exposure and risk reductions? The questions outlined above have been addressed in the REA. The following sections present considerations regarding the adequacy of the current standards and potential alternative standards, as discussed in chapter 10 of the REA, in terms of indicator, averaging time, form, and level. E. Adequacy of the current standards In considering the adequacy of the current standards, the policy assessment chapter of the REA considered the scientific evidence assessed in the ISA, as well as the air quality, exposure, [Text truncated at 120,000 characters. The full text is on the page linked above.] --- Source: Frix Law Library, https://www.frixlaw.com/law-library/documents/fr%3AE9-28058. Public record. Not legal advice.